Report of the task force on designing clinical trials in early (predementia) AD

Aisen, Paul S.; Andrieu, Sandrine; Sampaio, Cristina; Carrillo, María C.; Khachaturian, Zaven S.; Dubois, Bruno; Feldman, Howard; Petersen, Ronald C.; Siemers, Eric; Doody, Rachelle S.; Hendrix, Suzanne; Grundman, Michael; Schneider, Lon S.; Schindler, Rachel; Salmon, Éric; Potter, William Z.; Thomas, Ronald G.; Salmon, David P.; Donohue, Michael; Bednar, Martin M.; Touchon, Jacques; Vellas, Bruno

doi:10.1212/wnl.0b013e318207b1b9

Cited by 158 publications

(120 citation statements)

References 29 publications

(22 reference statements)

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“…Thus, there is an urgent need and interest to conduct clinical trials during the prodromal phase in patients with mild cognitive impairment (MCI), with the aim to prevent or at least delay the onset of dementia by disease-modifying intervention (1).…”

mentioning

confidence: 99%

Evaluation of a Calibrated ¹⁸F-FDG PET Score as a Biomarker for Progression in Alzheimer Disease and Mild Cognitive Impairment

Herholz

Westwood²,

Haense³

et al. 2011

J Nucl Med

104

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mentioning

confidence: 99%

Evaluation of a Calibrated ¹⁸F-FDG PET Score as a Biomarker for Progression in Alzheimer Disease and Mild Cognitive Impairment

Herholz

Westwood²,

Haense³

et al. 2011

J Nucl Med

104

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“…It was demonstrated that by inhibition PS1 and nicastrin (NCT), two components of γ-secretases, the cognitive function of APP/ PS1 Tg mice improved [39]. However, many researchers believe that the severity of cognitive impairment is more closely related to NTFs in the cortical nerves, which might be one of the possibilities that many clinical trial targeting Aβ failed [40,41]. Nevertheless it is undeniable that Aβ deposition plays a key role in the pathogenesis of AD [42].…”

Section: Neurotoxicity Of Aβmentioning

confidence: 99%

Application of APP/PS1 Transgenic Mouse Model for AlzheimerÃ¢ÂÂs Disease

Li¹,

Wei²,

Wang³

et al. 2015

J Alzheimers Dis Parkinsonism

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Alzheimer's disease (AD), the most common neurodegenerative disorder, will not only reduce quality of life severely, but also bring heavy economic burden to the family and society. Slow progress in AD therapies partially due to lack of appropriate animal models. APP/PS1 transgenic mouse, a widely used animal model for AD, can be used in lots of aspects for AD related study, such as neuronal apoptosis, inflammation, cholinergic abnormal, neurogenesis disorder and synaptic plasticity. Despite all this, APP/PS1 transgenic mice model is not a perfect model, and more suitable animal model according to the aim of research should be established. mutant, the APP KI mutation alone does not affect markers for adult hippocampal neurogenesis [12]. PS1 KI mice, a model that shows cognitive decline developed in an Aβ-independent way, therefore plaque-dependent pathology cannot be expected [13].Tg models are important models for the AD study. They are established on the basis of genetics, mainly involves amyloid precursor protein(APP) gene on chromosome 21, presenilin1 (PS1) gene on chromosome 14, presenilin 2 (PS2) gene on chromosome 1, Tau protein gene on chromosome 17 and Apolipoprotein E (ApoE) gene on chromosome 19 [14]. By transgenesis, the course of AD can be simulated steadily at molecular level. Meanwhile, this technique can produce many animals at the same time, so the reliability and repeatability of experimental results can be ensured. Tg models have three types: single transgenic models such as APP Tg mouse model, double Tg models such as APP/PS1 Tg mouse model and triple Tg mouse models such as APP/ PS1/Tau Tg mouse model [15]. Although the emergence of Tg model is a hot spot of AD research in recent years, there are still problems in the application of Tg AD models, such as lack of aging process, poor reproductive ability and immunity. Therefore, compared with the real AD pathological changes, there is still a long way to go. APP/PS1 Tg mouse model

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“…Several strategies for selection of subjects at risk are possible. Biomarkers including amyloid-β (Aβ) and tau in cerebrospinal fluid (CSF), structural MRI, functional imaging with FDG-PET and amyloid-imaging with Pib-PET have all been suggested as candidates for selection of subjects in clinical trials in early AD [54]. The use of such biomarkers aims to select a homogeneous population by defining a nosological entity (e.g.…”

Section: Target Populationmentioning

confidence: 99%

Methodological challenges in designing dementia prevention trials — The European Dementia Prevention Initiative (EDPI)

Richard¹,

Andrieu²,

Solomon³

et al. 2012

Journal of the Neurological Sciences

102

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Report of the task force on designing clinical trials in early (predementia) AD

Cited by 158 publications

References 29 publications

Evaluation of a Calibrated ¹⁸F-FDG PET Score as a Biomarker for Progression in Alzheimer Disease and Mild Cognitive Impairment

Evaluation of a Calibrated ¹⁸F-FDG PET Score as a Biomarker for Progression in Alzheimer Disease and Mild Cognitive Impairment

Application of APP/PS1 Transgenic Mouse Model for AlzheimerÃ¢ÂÂs Disease

Methodological challenges in designing dementia prevention trials — The European Dementia Prevention Initiative (EDPI)

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Report of the task force on designing clinical trials in early (predementia) AD

Cited by 158 publications

References 29 publications

Evaluation of a Calibrated 18F-FDG PET Score as a Biomarker for Progression in Alzheimer Disease and Mild Cognitive Impairment

Evaluation of a Calibrated 18F-FDG PET Score as a Biomarker for Progression in Alzheimer Disease and Mild Cognitive Impairment

Application of APP/PS1 Transgenic Mouse Model for AlzheimerÃ¢ÂÂs Disease

Methodological challenges in designing dementia prevention trials — The European Dementia Prevention Initiative (EDPI)

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Evaluation of a Calibrated ¹⁸F-FDG PET Score as a Biomarker for Progression in Alzheimer Disease and Mild Cognitive Impairment

Evaluation of a Calibrated ¹⁸F-FDG PET Score as a Biomarker for Progression in Alzheimer Disease and Mild Cognitive Impairment

Application of APP/PS1 Transgenic Mouse Model for AlzheimerÃ¢ÂÂs Disease